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Allergy and Immunology Board Review

Allergy and Immunology Board Review. Most of this power point was prepared by Drew White. Basic Immunology Asthma Eosinophilic Lung Disease Allergic Rhinitis Sinusitis Atopic Dermatitis Urticaria. Autoimmune Blistering Skin Diseases Mastocytosis Hypereosinophilia Syndrome Food Allergy

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Allergy and Immunology Board Review

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  1. Allergy and Immunology Board Review

  2. Most of this power point was prepared by Drew White.

  3. Basic Immunology Asthma Eosinophilic Lung Disease Allergic Rhinitis Sinusitis Atopic Dermatitis Urticaria Autoimmune Blistering Skin Diseases Mastocytosis Hypereosinophilia Syndrome Food Allergy Anaphylaxis Drug allergy Immunodeficiency Topics

  4. Basic Immunology • Innate Immune System • Complement, Neutrophils, Monocytes • Skin, mucosal surfaces • Adaptive Immune System • T cells, B cells, Antigen presenting cells • Antibodies

  5. Two ways to fire a Mast Cell • Cross link specific IgE on the surface • Directly disrupt the Mast Cell • Physically (think dermatographism) • Pharmacology (think morphine) • Chemically

  6. For ANY allergic/immunologic reaction you need…. • Previous exposure. • Antigen presenting cells find antigen • APC present antigen to T cells • T cells either KILL (antiviral) or HELP the B Cell make antibody (bacteria, allergy) • B cells start with IgM, later make IgG, IgA, IgE (called class switching)

  7. Gell and Coombs Classification • I – IgE on Mast cells – anaphylaxis • II – antigens on cell surface lead to cell destruction (IgG) – PCN binds to RBC, IgG binds to PCN/RBC and RBC destroyed • III – soluble antigen  Ag:Ab aggregates (immune complexes) deposit in tissues (serum sickness) • IV – T cell mediated. Direct T cell toxicity (PPD, Poison Ivy)

  8. Asthma • Asthma cases doubled from 6.8 mil in 1980 to 17.3 million in 1998 • Prevalence increasing by 5% per year • Rates about double in Puerto Ricans compared with other hispanic populations

  9. Asthma Diagnosis • FEV1 improvement of 12% and 200mL after beta-agonist is evidence for asthma according to ATS • Decreased FEV1/FVC ratio • 20-39yr 85% • 40-59yr 80% • 60-80yr 70% • Methacholine challenge – • + with 20% decrease FEV1 with <8-16mg/mL • True benefit is in negative predictive value

  10. Asthma Controllers • Inhaled steroids • Long acting beta agonists • Leukotriene antagonists • Xolair (omalizumab) • Systemic steroids

  11. Risk Factors for Asthma Death • Previous life-threatening asthma, respiratory arrest • Hospitalization or ED visit for asthma within the last year • Use of 2 or more canisters of rescue inhaler/month • Poor perception of hypoxia or airway obstruction • Psychosocial disturbance

  12. Pregnancy and Asthma • 1/3 worsen, 1/3 improve, 1/3 no change • Treatment – short answer, better to treat asthma than not to. Inhaled steroids and beta agonists generally felt to be safe. • Pulmicort is class B, other ICS class C • Avoid decongestants, epinephrine

  13. Variable extrathoracic Variable intrathoracic Fixed obstruction

  14. Expiratory Intrathoracic Obstruction “I” “E” Inspiratory Extrathoracic Obstruction “E” “I” E:I or I:E

  15. Differential Diagnosis • Extrathoracic • Laryngomalacia, tracheomalacia • Vocal cord pathology including VCD • Intrathoracic • Tracheomalacia of intrathoracic airway • Bronchogenic cysts • Tracheal tumor (malignant)

  16. Fixed upper airway obstruction • Tracheal stenosis • Goiter compressing

  17. Things to consider in the out of control asthmatic • Vocal cord dysfunction – episodes of dyspnea, inspiratory stridor, dysphonia • GERD • Sinusitis • Churg-Strauss syndrome • ABPA • Compliance/technique

  18. Hypersensitivity Pneumonitis • Also known as “extrinsic allergic alveolitis” • Acute, subacute, chronic • Fevers, chills, malaise, cough • CXR/CT scan abnl • Chronic  pulmonary fibrosis

  19. Hypersensitivity Pneumonitis (High yield) • Farmer’s lung – moldy hay – Saccharopolyspora rectivirgula • Pigeon Breeder’s disease – parakeets, parrots, pigeons – avian proteins • Malt workers lung – Moldy barley – aspergillus fumigatus and clavis

  20. Hypersensitivity Pneumonitis • Hot tub lung – mycobacterium avium complex • Cigarette smoking DECREASES risk of HP

  21. Occupational Asthma • Basically, asthma occurring because of exposure at work. • Testing difficult, so sometimes need to do pulmonary evaluation at the workplace. • Earlier you diagnose the better, because may lead to permanent asthma even when removed from environment.

  22. Tends to lead to persistent asthma Occupational Asthma

  23. Eosinophilic Lung Disease • Acute eosinophilic pna • Chronic eosinophilic pna • ABPA • Churg Strauss

  24. Acute eosinophilic pna • Young healthy individuals • Present within days • Low/absent peripheral eos • High pulm eos • Bronch needed • Universally respond to steroids

  25. Chronic eosinophilic pna • Subacute presentation • 50% have history of asthma • Photographic negative of pulm edema on chest film • Peripheral eos normal

  26. ABPA • Criteria • Asthma • High total IgE (>1000 ng/mL or 417 kU/L) • Positive skin test to A. fumigatus • Elevated specific IgE to A. fumigatus • If CT with central bronchiectasis then ABPA-CB, otherwise ABPA-S (seropositive)

  27. Stages • Stage I – acute phase • Stage II – remission • Stage III – exacerbation • Stage IV – steroid dependent • Stage V – pulmonary fibrosis

  28. Treatment • Steroids for acute flares • Follow IgE and CXR • Itraconazole as steroid sparing agent, long term studies not yet in

  29. (A), shows a non-homogeneous consolidation (short arrow) in right mid-zone. Left perihilar infiltrates simulating hilar adenopathy (arrowhead) along with parallel-line opacities in the left mid-zone (long arrow) are also visible. (B) taken after seven weeks shows significant clearing of the nonhomogeneous consolidation in the right mid-zone. Left perihilar infiltrates are still present while a new ‘toothpaste-shadow’ has appeared exactly at the site of the parallel-line opacities seen in (A). (C) taken after a further twelve weeks shows reappearance of the consolidation in the right upper and mid-zones (arrow) with partial clearing of the left perihilar infiltrates.

  30. Churg- Strauss Syndrome • Transient patchy interstitial infiltrates • Fever • Weight loss • Elevated ESR • Abnormal LFT • Peripheral eosinophilia (>1000/micL) • pANCA + 50-75% of cases

  31. Mimics of Allergic Rhinitis • Nasal manifestations of systemic disease: • Diabetes mellitus – mucor • Wegener’s granulomatosis • Midline granuloma • Relapsing polychondritis • Sarcoidosis • Cystic fibrosis • CSF leak – check beta 2 transferrin (very specific) • Vasomotor rhinitis, rhinitis medicamentosa

  32. Allergic Rhinitis • Increases chances that truly allergic rhinitis • Longstanding • Seasonal peaks, triggers (pets, grass…) • Nasal pruritus, sneezing, congestion, post nasal drip, rhinorrhea • Eye features (watering, pruritic, injected) • Family history

  33. Lab Evaluation • Skin testing with highest sens/spec • RAST test – in vitro test ~85-90% sens • Good for those on antihistamines • Diffuse dermatitis with no normal skin to test

  34. Allergic Rhinitis • Nasal steroids – first line • Antihistamines and leukotriene receptor antagonists – second line

  35. Immunotherapy • Indicated for severe symptoms, usually not responding to medical management and avoidance of allergen • Duration of 3-5 years • Therapeutic effect after 3-5 years usually permanent • Approved for allergic rhinitis, asthma, venoms. Less effective for things like AD

  36. Nasal Polyps/Chronic Sinusitis • Anosmia – big tip off • Causes: idiopathic, immunodeficiency, CF • Can be associated with Aspirin Triad: • Chronic sinusitis/ nasal polyposis • Asthma • Exacerbation with ASA / NSAID product

  37. Treatment • Treat underlying disease if present • Systemic, topical steroids • Leukotriene antagonists • Surgical debulking • For ASA triad – ASA desensitization is proven to improve outcomes.

  38. Atopic Dermatitis • Increased susceptibility to • Staph aureus, HSV(eczema herpeticum), vaccinia • Usual affected areas – flexural aspects of extremities, hands • Need to rule out cutaneous T – cell lymphoma in an adult presenting with eczematous dermatitis

  39. Treatment • Skin hydration/moisturization • Topical corticosteroids • Oral antibiotics (Staph) • Antihistamines (control itch) • Topical calcineurin inhibitors (protopic/ elidel)

  40. Urticaria and Angioedema • <6 weeks – acute, usually find the cause • >6 weeks – chronic, unusual to find cause • Physical urticarias – cold, heat, cholinergic, delayed pressure, dermatographism, solar

  41. Urticaria – Look for • Pruritic, erythematous lesions that blanch • Lesion duration <24 hours • Can be papules or plaques • May have exacerbation with NSAIDs

  42. Urticaria - Treatment • Daily non-sedating antihistamine is first line therapy • Second line agents are H2 blockers, leukotriene modifiers (Montelukast) • Some may need oral steroid burst • For chronic urticaria, some require oral steroids or other immunomodulators

  43. Chronic Urticaria • Not usually allergen driven • 30% have autoantibodies to high affinity IgE receptor or to IgE • Thyroid autoimmunity higher than controls

  44. Hiveless Angioedema • Hereditary or Acquired • More likely to have angioedema precipitated by trauma • Dental visit • Classic board ? Is genital edema in child riding bike • Visceral attacks – many undergo appy for acute abdomen, but normal appendix.

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